Cited by 108Attention Deficit Hyperactivity DisorderNeurotransmitter Receptor Influence on BehaviorGenetics and Neurodevelopmental Disorders

Association analysis of monoamine oxidase A and attention deficit hyperactivity disorder

Lawson, Deborah C., Turic, Darko, Langley, Kate, Pay, Helen M., Govan, Catherine F., Norton, Nadine, Hamshere, Marian L., Owen, Michael J. +2 more·2003·American Journal of Medical Genetics Part B: Neuropsychiatric Genetics

Abstract

Attention deficit hyperactivity disorder (ADHD) is a highly heritable disorder. Although the causes of ADHD are unknown, dopaminergic, serotonergic and nor‐adrenergic pathways have been strongly implicated. Monoamine Oxidase A (MAOA) is involved in the degradation of all three of these neurotransmitters and therefore has been suggested as a strong candidate gene for ADHD. Animal and human studies have implicated MAOA and 5‐HT in impulsive and aggressive behavior. We therefore additionally postulated that MAOA might be associated with a subtype of ADHD where aggressive and impulsive features are especially prominent. We have tested this hypothesis by genotyping two polymorphisms (the 30‐bp VNTR in the promoter and the Fnu4HI 941T→G) in MAOA that are associated with altered MAOA function. Our sample consisted of 171 British Caucasian children 6–16 years of age fulfilling DSM‐III R, DSM‐IV or ICD‐10 criteria for ADHD/Hyperkinetic Disorder. Using case control analysis and then the TDT, no association was found between these two MAOA polymorphisms and ADHD. Case control analysis of the VNTR showed an association with a subgroup of children with comorbid conduct problems (OR = 2.0, 95% CI = 1.09, 3.5), and TDT analysis indicated a statistical trend toward association. Our findings highlight the importance of phenotype definition and the need for the MAOA VNTR to be further examined. © 2003 Wiley‐Liss, Inc.

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Crossref · 10.1002/ajmg.b.10002

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  • The first study investigating MAOA-uVNTR and childhood aggressive behavior in the context of ADHD reported that low transcription (3 R only) alleles were associated with higher aggression among children with ADHD.

    “The first study that investigated the association between MAOA-uVNTR and childhood aggressive behavior in the context of ADHD reported that low transcription (3 R only) alleles of MAOA-uVNTR was associated with higher aggression among children with ADHD [43].”

    From Genetics of child aggression, a systematic review (2024) · cites this paper as [43]

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Authors
Lawson, D. C., Turic, D., Langley, K., Pay, H. M., Govan, C. F., Norton, N., Hamshere, M. L., Owen, M. J., O'Donovan, M. C., & Thapar, A.
Affiliations
University of Wales (GB)
Corresponding author
Thapar, Anita
Venue
American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
Publisher
Wiley
Published
2002-12-19
Volume
116B
Issue
1
Pages
84-89
ISSN
  • 1552-4841 (ISSN-L)
  • 1552-485X
OpenAlex
W2062199416
Cited by
108
References
34
Citations by year
2025: 3 · 2024: 1 · 2023: 1 · 2022: 3 · 2020: 3 · 2019: 3 · 2018: 2 · 2017: 1 · 2016: 2 · 2015: 2 · 2014: 9 · 2013: 2 · 2012: 4
FWCI
2.75
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Medical Genetics Part B Neuropsychiatric Genetics (publishedVersion)
  • PubMed (publishedVersion)
  • ePrints Soton (University of Southampton) (submittedVersion)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Keywords
attention deficit hyperactivity disorder, monoamine oxidase A, conduct problems, candidate gene association, hyperkinetic disorder, children, phenotype definition
MeSH terms
Adolescent, Alleles, Attention Deficit Disorder with Hyperactivity, Child, DNA, Gene Frequency, Genotype, Humans, Monoamine Oxidase, Case-Control Studies, Minisatellite Repeats, Polymorphism, Single Nucleotide

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